Background and Purpose-Many patients with acute stroke are excluded from receiving thrombolysis agents within the necessary time limit (3 or 6 hours from stroke onset) because they or their family members are unable provide the time of stroke onset. Brain tissue sodium concentration ([Na ϩ ]) increases gradually and incessantly during the initial hours of experimental focal cerebral ischemia but only in severely damaged brain regions. We propose that this steady increase in [Na ϩ ] can be used to estimate the time after arterial occlusion in the rat middle cerebral artery occlusion model of ischemic stroke. Methods-Sixteen anesthetized Sprague-Dawley rats underwent permanent middle cerebral artery occlusion combined with bilateral common artery occlusion. After 100 to 450 minutes, diffusion-weighted MRI was used to generate apparent diffusion coefficient (ADC) maps, cerebral blood flow (CBF) was determined with 14 C-iodoantipyrine (in a subset of 7 animals), and the brain was frozen. Autoradiographic CBF sections and punch samples for Na ϩ analysis were obtained from the brain at the same level of the MR image. Severely at risk regions were identified with an ADC of Ͻ520 m 2 /s and, in the subset, with both ADC of Ͻ520 m 2 /s and CBF of Ͻ40 mL ⅐ 100 g Ϫ1 ⅐ min

Enterovirus 71(EV71) causes recurring outbreaks of hand, foot and mouth disease and encephalitis leading to complications or death in young children. More effective antiviral drugs are needed to prevent or reduce EV71-related disease and complications. However, there are no standard models currently in use to evaluate activity against EV71 infection both in vitro and in vivo. In this study, the activity of ribavirin and pleconaril against EV71 infection was evaluated in two models. An in vitro EV71 infection model was developed in RD cells, and an in vivo EV71 infection model was applied. Ribavirin and pleconaril effectively increased the viability of infected cells. Pleconaril reduced the morbidity and mortality of one-day-old infected mice, but ribavirin did not protect the infected mice. In all, the results demonstrated that infected cells and infected mice can be used to evaluate antiviral activity of ribavirin and pleconaril against EV71 infection in vitro and in vivo.

The etiology of glioma remains unclear so far. Human herpesvirus 6 (HHV-6) might be associated with glioma, but there is no direct evidence to support this. High percentages of HHV-6 DNA and protein were detected in tissue from gliomas, compared with normal brain tissue. In addition, a strain of HHV-6A was isolated from the fluid specimens from glioma cysts. High levels of interleukin 6 (IL-6), interleukin 8 (IL-8), tumor necrosis factor α, and transforming growth factor β (TGF-β) were detected in the cyst fluid specimens from HHV-6-positive patients with glioma. Furthermore, HHV-6A infection promoted IL-6, IL-8, and TGF-β production in astrocyte cultures. Our studies strongly suggest the involvement of HHV-6 infection in the pathogenesis of glioma.